We are proposing to extend our discovery of increased renal alpha-adrenergic (vasoconstrictor and salt retaining) receptors in the rat (SH) model of human essential hypertension. This will be done by 1) studying the long-term effect of alpha-receptor number suppression by phenoxybenzamine in the model 2) determining whether this abnormality occurs in humans by a) studying renal tissue obtained at surgery and from trauma victims b) establishing the techniques of measuring alpha-receptors in platelets of hypertensives vs. normotensives and 3) extending our techniques of quantifying alpha-receptors to more specific agents including radiolabelled yohimbine (alpha 2) and prazosin (alpha 1). We are also extending our studies to measurement of renal alpha-receptors in the sodium sensitive and sodium resistant strains of Dahl hypertensive rats. This will be done with low and high sodium diets to see if hypertension is correlated with the abnormal alpha-receptors. If the abnormal alpha-receptors are present in the kidneys of this strain we will attempt quantification and characterization of the alpha-receptors in the spleen and salivary glands to determine the organ specificity of this abnormality.